During recent years, dipeptidyl peptidase-4 (DPP-4) inhibition has been included in the clinical management of type2 diabetes, both as monotherapy and as add-on to several other therapies. DPP-4 inhibition prevents the inactivation of the incretin hormones, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1). This results in stimulation of insulin secretion and inhibition of glucagon secretion, and there is also a potential β-cell preservation effect, as judged from rodent studies; that is, it might target the key islet dysfunction in the disease. In type2 diabetes. This reduces 24-h glucose levels and reduces HbA 1c by ≈0.8-1.1% from baseline levels of 7.7-8.5%. DPP-4 inhibition is safe, with a very low risk for adverse events including hypoglycemia, and it prevents weight gain. The present review summarizes the studies on the influence of DPP-4 inhibition on islet function. © 2011 Asian Association for the Study of Diabetes and Blackwell Publishing Asia Pty Ltd.
CITATION STYLE
Ahrén, B. (2012, February). DPP-4 inhibition and islet function. Journal of Diabetes Investigation. https://doi.org/10.1111/j.2040-1124.2011.00184.x
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